August 1, 1999AJP Heart and Circulatory Physiology
Human heart failure: cAMP stimulation of SR Ca2+-ATPase activity and phosphorylation level of phospholamban
Key result
Failing human myocardium exhibited a 20 +/- 2% decrease in the cAMP-dependent phosphorylation level of phospholamban and decreased responsiveness to direct activation of SR Ca(2+)-ATPase activity.
Population
Failing human myocardium (end-stage heart failure) and nonfailing human myocardium
Comparison
Direct activation of SR Ca-ATPase activity by… vs Nonfailing human myocardium
Design
Preclinical
Authors
Discussion
Loading...
Member takes
Implication
No immediate clinical implications in HF; leaves open phospholamban phosphorylation as a mechanistic target for future studies.
Structured PICO
P
Population
Failing human myocardium (end-stage heart failure) and nonfailing human myocardium
E
Exposure
Direct activation of SR Ca(2+)-ATPase activity by cAMP (0.01-100 micromol/l) or protein kinase A (1-30 microgram)
C
Comparator
Nonfailing human myocardium
O
Outcome
SR Ca(2+)-ATPase activity and cAMP-dependent phosphorylation level of phospholambansurrogate
Impaired sarcoplasmic reticulum function in end-stage human heart failure may be partly due to reduced cAMP-dependent phosphorylation of phospholamban rather than changes in protein expression.
Cite This Study
Schmidt et al. (1999) studied Human heart failure. Failing myocardium vs. Nonfailing human myocardium was evaluated on cAMP-dependent phosphorylation level of phospholamban. Failing human myocardium exhibited a 20 +/- 2% decrease in the cAMP-dependent phosphorylation level of phospholamban and decreased responsiveness to direct activation of SR Ca(2+)-ATPase activity.